Nonobstructive Acute Pyelonephritis Presenting as Acute Renal ...

J Med Sci 2003;23(1):61J64
http://jms.ndmctsgh.edu.tw/2301061.pdf
Copyright © 2003 JMS
Nonobstructive Acute Pyelonephritis Presenting
as Acute Renal Failure in the Elderly
Yuen-Hua Ni 1 , Ning-Chi Wang 1 , Ann Chen 2 , Yuh-Feng Lin 3 , and Feng-Yee Chang 1*
1 Division of Infectious Diseases and Tropical Medicine, Department of Medicine,
2 Department of Pathology, 3 Division of Nephrology, Department of Medicine,
Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan, Republic of China
Received: May 16, 2002; Revised: July 17, 2002; Accepted:
July 23, 2002.
* Corresponding author: Feng-Yee Chang, Division of Infectious
Diseases and Tropical Medicine, Department of
Medicine, Tri-Service General Hospital, 325, Chung-Kung
Road Section 2, Taipei 114, Taiwan, Republic of China. Tel:
+886-2-87927257; Fax: +886-2-87927258; e-mail :
fychang@ndmctsgh.edu.tw
Yuen-Hua Ni, et al.
Acute renal failure is a rare, but less recognized complication of acute bacterial pyelonephritis in patients who do not
have urinary obstruction. We describe an aged woman who developed acute renal failure suffered from severe bilateral
flank pain for one week and progressive anorexia, general weakness, decreased urine output and short of breath. She
did not have hypotension, fever, leukocytosis and thrombocytopenia. Urinalysis showed numerous leukocytes in the
urine. Biochemistry revealed marked renal function impairment with BUN 98 mg/dL and creatinine 7.2 mg/dL.
Abdominal sonography demonstrated bilateral enlarged kidney without the evidence of obstruction. Blood and urine
cultures grew Escherichia coli. The renal biopsy revealed predominant leukocyte filtration in the interstitium and
tubules, compatible with acute pyelonephritis. Antimicrobial therapy and hemodialysis led to rapid improvement in
clinical symptoms and renal function. The clinician should be aware that acute bacterial pyelonephritis can cause acute
renal failure in the elderly even with no urinary obstruction and hypotension.
Key words: acute renal failure, bacteremia, pyelonephritis
INTRODUCTION
Acute renal failure is commonly seen in hospitalized
patients. Based on the anatomical site of involvement, it
can be classified into postrenal, prerenal and renal. Renal
sites of involvement can be subdivided into vascular,
glomerular, interstitial, and tubular lesions. Infection-related
acute renal failure is usually related to septic shock,
urinary tract obstruction, immune-mediated glomerular or
tubulointerstitial nephritis, and direct bacterial invasion 1,2 .
Although urinary tract infections are common in the elderly,
acute pyelonephritis without an association of obstruction
and hypotension is rarely considered in the differential
diagnosis of acute renal failure 3,4 . Herein, we report on the
case of an elderly woman with no urinary tract obstruction
who developed acute bacterial pyelonephritis with acute
renal failure requiring hemodialysis support.
CASE REPORT
An 82-year-old female was admitted to our hospital
with a 1-week history of bilateral flank pain, back pain and
progressive lassitude, decreasing urine output and shortness
of breath. There was no history of fever, chills, or
dysuria. She also denied any history of previous urinary
tract infection. She was noted to have a serum creatinine of
1.0 mg/dL and BUN 11 mg/dL six months ago. However,
she had been using a nonsteroidal anti-inflammatory drug
(ibuprofen) to control back pain for one week prior to
admission.
On admission, her blood pressure was 120/70 mmHg,
pulse rate 88/minute, respiration 20/minute and temperature
36.5 o C. On physical examination she was lethargic but
arousable. Her mucous membranes appeared dry. Lungs
were clear to auscultation and examination of the heart
revealed a normal sinus rhythm, with grade II systolic
ejection murmur. There was no gallop or pericardial rub.
Abdomen was soft with marked knocking tenderness over
bilateral costo-vertebral angle. There was no pitting edema.
Complete blood count showed white blood cell count
(WBC) 11,200/uL, with 87% segmented neutrophils
predominant, hemoglobin 8.4 g/dL, hematocrit 25.3%,
platelet count 176,000/uL. Urinalysis revealed a pH of 5.5,
protein (2+), no eosinophiluria, positive reaction for nitrates,
and numerous WBC/HPF. Urine Bence-Jones protein was
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Acute pyelonephritis and acute renal failure
negative. Her blood urea nitrogen (BUN) was 98 mg/dL,
creatinine 7.2 mg/dL, serum sodium 135 mmol/L, potassium
4.8 mmol/L, chloride 96 mmol/L, total serum calcium
7.4 mg/dL, phosphate 5.2 mg/dL, cholesterol 164
mg/dL, total protein 6.1 g/dL, and albumin 3.4 g/dL. Liver
function was normal. Serum c-reactive protein (CRP) was
elevated at 9.5 mg/dL. Arterial blood gases revealed pH
7.335, PCO 2 26.6 mmHg, PO 2 84.8 mmHg, HCO 3 13.9
mmol/L. Serum iron and TIBC levels were 46 g/dL and
212 mg/dL, respectively. Serum ferritin concentration was
540 ng/L. Immunological studies showed normal C3, C4,
IgM, IgA, ASOT, RF and negative ANA except mildly
increased serum IgG levels (1,670 mg/dL). Tumor markers
were normal . Chest X-ray revealed cardiomegaly and
torturosity of the aorta. KUB demonstrated bilateral enlarged
kidney shadow, severe degenerative joint disease
and osteoporosis. A renal ultrasound indicated increased
size of kidneys bilaterally (right kidney: 12 cm, left kidney
11.8 cm) and increased echogenicity, without evidence of
obstruction.
This initial impression was urinary tract infection with
sepsis and acute renal failure although she had no fever.
Intravenous flumarine 1.0 gm every 8 hours was initiated
along with volume repletion with 1 liter normal saline.
Nevertheless, renal function remained severely impaired
and urine output was still oligouric despite hydration and
antibiotic therapy. Since she progressed to shortness of
breath, vomiting, anorexia, and severe metabolic acidosis,
hemodialysis was started on hospital day 3. A diagnostic
percutaneous renal biopsy was performed on hospital day
5. Light microscopic examination of the renal biopsy
showed a predominant neutrophil infiltration in the interstitium
and renal tubules. Occasional intratubular neutrophils
were also seen. The glomeruli and vessels appeared
normal. Immunofluorescent staining for IgG, IgA, IgM,
C3, C1q, and fibrinogen was negative. Cultures of urine
and blood raised Escherichia coli. By the end of the first
week, her serum creatinine began to decline, and with
improving urine routine and negative urine and blood
cultures, dialysis was discontinued on day 9. She required
a total of four hemodialysis treatments. During her hospital
stay, the patient remained afebrile. At the time of discharge
on hospital day 12, her BUN was 24 mg/dL and serum
creatinine 1.5 mg/dL.
DISCUSSION
The patient presented above showed many of the signs
and symptoms of acute pyelonephritis with acute renal
failure. She had typical presentations such as bilateral
62
Fig. 1 Renal biopsy showing a diffuse prominent polymorphonuclear
leukocyte infiltration in the interstitium
and renal tubules in high power field. WBC casts were
present in the lumen of renal tubules.
flank pain, enlarged kidneys, along with a positive urine
and blood culture. These distinct features have been noted
frequently in earlier case reports 5,6 . However, she lacked
hypotension, any fever, leukocytosis, and thrombocypenia
despite the presence of severe bacteremia. In addition, no
predisposing factors such as a structural abnormality of the
urinary tract, indwelling catheter, solitary kidney or renal
transplant were identified in this patient 7-9 . Finally, compared
with the more common pattern of ischemic or toxininduced
acute renal failure, the recovery of acute renal
failure due to acute pyelonephritis appears to be almost
complete and much quicker 10 . Consistent with previous
reports, most of all cases occurred in individuals with no
history of urinary tract infections were caused by Escherichia
coli. Nevertheless, acute oligouric renal failure associated
with bacterial pyelonephritis is still an ignored and
unrecognized clinical entity.
The pathogenesis of acute renal failure associated with
acute pyelonephritis in this patient remains uncertain. True
extracellular fluid volume depletion was not a major contributing
factor because volume repletion did not reverse
her oligouria and renal function. Acute tubular necrosis
may occur in systemic bacteremia without the accompaning
hypotension through the actions of vasoactive hormones,
endotoxins, and cytokines that cause intrarenal
vasoconstriction 11,12 . Although intrarenal vasoconstriction
due to bacteremia could not be completely ruled out, the
predominant interstitial edema, microabscess formation,
leukocyte interstitial infiltration and tubular obstruction by
cellular debris demonstrated by the renal biopsy favored
that bacterial pyelonephritis directly caused renal function
in both kidneys. Furthermore, acute bacterial pyelonephritis
per se may result in the reduction of the glomerular
filtration rate secondary to high hydrostatic pressures within
the renal interstitium 13 .

This patient had no prior history of renal disease and
was taking an NSAID at the time of presentation. NSAID
use is a well-known cause of both acute and chronic renal
failure 14 . The chronic case usually involves the development
of papillary necrosis resulting from the habitual
consumption of NSAIDs 15 . The acute scenario is either
NSAID-induced hemodynamic deterioration of renal function
or NSAID- associated tubulointerstitial nephritis 16 .
The latter is commonly accompanied by nephrotic syndrome
whereas the former often needs risk factors plus a
higher dose of NSAIDs and usually develops with typical
acute tubular necrosis. Although the possibility of NSAIDinduced
acute renal failure can not be entirely excluded, the
typical findings of acute pyelonephritis from renal biopsy
mitigate against both NSAID-induced hemodynamic and
immune-mediated acute renal failure.
Acute renal failure associated with enlarged kidney in
the absence of obstruction is usually associated with infection
(leptospirotis, HIV infection, malacoplakia, et al.),
tumor-infiltration (multiple myeloma, leukemia and
lymphoma), diabetic mellitus, nephrotic syndrome (focal
segment glomerulosclerosis), renal vein thrombosis, or
drugs (heroins). In this case, enlargement of the kidneys is
typically associated with acute bacterial pyelonephritis.
Enlarged kidneys associated with anemia, back pain and
acute renal failure seen in this patient are also the common
clinical presentations in multiple myeloma. However, the
immune study and no evidence of M protein in the plasma
did not favor the possibility of multiple myeloma.
In conclusion, the present case highlights the fact that
acute bacterial pyelonephritis alone can result in an uncommon
but serious complication of acute renal failure,
which requires hemodialytic intervention in the elderly
with no urinary tract obstruction. It should be stressed that
acute bacterial pyelonephritis even without hypotension
should be kept in the differential diagnosis of acute renal
failure. Rapid diagnosis and treatment can lead to a more
complete recovery of renal function.
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